This document discusses electrolyte imbalances in children. It begins by defining electrolyte disturbances as imbalances in ions like sodium, potassium, chloride, and bicarbonate in the blood. It then explains that electrolyte disturbances in children are often caused by gastrointestinal illnesses like diarrhea or vomiting, or renal diseases. The majority of the document then focuses on providing in-depth information on the etiology, clinical manifestations, diagnosis, and management of specific electrolyte imbalance conditions like hyponatremia, hypernatremia, hypokalemia, and hyperkalemia.

1. An electrolyte disturbance
is an imbalance of certain ionized salts (i.e., bicarbonate, calcium,
chloride, magnesium, phosphate, potassium, and sodium) in the blood.
Electrolytes are substances that are found in the ICF and ECF, they
might be positively charged such as Na+ and K+, or negatively charged
such as Cl- and HCO3-.
Fluid and electrolyte disturbances in children commonly are the result
of gastrointestinal illness (i.e., diarrhea, vomiting, or both) and renal
diseases.
1

2. 2

3. Hyponatremia:
A common electrolyte imbalance, abnormally low plasma
sodium concentration below 136 or 135 mmol/L (mEq/L).
Hypovolemic Euvolemic Hypervolemic
(Water excess >
sodium excess)
(Modest ECF volume
excess, no edema)
(Sodium losses > water
losses)
Etiology:
3

4. 4

5. 5

6. 6

7. 7

8. 8

9. 9

10. Hypovolemic:
Renal losses:
 Prematurity
 Recovery phase of AKI
 Diuretics
 Osmotic diuresis
 salt-wasting nephropathy
 Bicarbonates
 Renal tubular acidosis
 Metabolic alkalosis
 Adrenal insufficiency
 Pseudohypoaldosteronism
 Cerebral salt-wasting syndrome
Extra renal loss:
Gastrointestinal
 Vomiting
 Diarrhea
 Sweating (cystic
fibrosis)
 Pancreatitis
 Burns
 Muscle trauma
 Peritonitis
 Effusions
Etiology:
10

11. Euvolemic:
Excess ADH (SIADH) , Reset osmostat, Glucocorticoid
deficiency, Hypothyroidism, Water intoxication, IV therapy,
Tap water enema, Infants fed excessive water.
Hypervolemic:
- Edema causing diseases such as (congestive heart failure,
chronic liver diseases -cirrhosis-, and nephrotic syndrome).
- Renal failure (acute or chronic).
Etiology:
11

12. Clinical Manifestations:
- Asymptomatic in chronic hyponatremia
- Brian swelling: due to shift of fluid into tissues
- Neurological manifestation:
anorexia, nausea, emesis, malaise, lethargy, confusion,
agitation, headache, seizures, coma, and decreased
reflexes.
- Other symptoms:
Cheyne-Stokes respirations, muscle cramps, and
weakness.
- symptoms of underlying cause
12

13. 13
Diagnosis:
- Detailed history: for detect the cuase
- Full examination (look for the signs of dehydration or fluid overload,edema,vital signs).
- Investigations:
- Serum Na level:
- -plasma osmolality: low in hyponatremia
- Urine sodium level : >20meq/L in SIADH ,<20MEQ/L in hypovolemia
- Urinary osmolality: <100mosm/kg =diluted urine in too much fluid
- >100mosm/kg =concentrated urine in SIADH ,hypothyrodism
- Others: electrolyte assay, RFT ,, Blood glucose, urine specific gravity, Blood urea, potassium, calcium,
magnesium, and phosphate

14. • Avoiding more than a 12-mEq/L increase in the serum
sodium every 24 hours is prudent, especially in chronic
hyponatremia.
• Treatment of hypovolemic hyponatremia requires
administration of IV fluids with sodium to provide
maintenance requirements and deficit correction, and to
replace ongoing losses.
Management of hyponatremia
14

15. • Emergency treatment of symptomatic hyponatremia, such as
seizures uses IV hypertonic saline to rapidly increase the serum
sodium concentration, which leads to a decrease in brain
edema.
• One milliliter per kilogram of 3% sodium chloride increases the
serum sodium by approximately 1 mEq/L. A child often
improves after receiving 4-6 mL/kg of 3% sodium chloride.
15

16. Hypernatremia:
A common electrolyte imbalance, abnormally increases in the
plasma concentration of sodium above 145 mmol/L (mEq/L).
Etiology of hypernatremia:
1- Excessive Sodium:
• Excess sodium bicarbonate
• Ingestion of seawater or sodium chloride
• Intentional salt poisoning
• Intravenous hypertonic saline
• Hyperaldosteronism
16

17. 2-Water loss:
-Low Urine Osmolality:
• Nephrogenic diabetes insipidus
• Central diabetes insipidus
-High Urine Osmolality:
• Premature infants
• Phototherapy
• Ineffective breastfeeding
• Adipsia (lack of thirst)
-Low Urine Output:
• Diarrhea
• Emesis
• Osmotic cathartics (lactulose)
• Burns
• Excessive sweating
-High Urine Output
• Osmotic diuretics (mannitol)
• Diabetes mellitus
• Chronic kidney disease
• Polyuric phase of acute
• tubular necrosis
3- Water and Sodium loss
Etiology:
17

18. • 1-Dehydration:
• Most children with hypernatremia are dehydrated and
have the typical signs and symptoms of dehydration ,
due to shifting of water from intracellular space to
extracellular space .
Clinical Manifestations:
18

19. 19
• 2-CNS symptoms :
a- Patients are irritable, restless, weak, and lethargic , some infant
have some infant have high pitched cry and hyperpnoea .
b- Some infants have a high-pitched cry and hyperpnoea .
c - Hypernatremia may cause fever.
d- Alert patients are very thirsty , although nausea may be present .
e- Brain hemorrhage is the most devastating consequence of
hypernatremia tearing of intracerebral veins , it occur due to
f- Seizures and coma are possible sequelae of the hemorrhage.

20. Diagnosis:
-Detailed history.
- Full examination.
Investigations:
-Serum Na+ level.
-Urine Na+ level.
-RFT.
-ADH level.
20

21. • Follow serum sodium concentration and adjust fluid
based on clinical status .
• Detect the underlying cause, strict sodium intake,
frequent monitoring of serum Na+, assess and
correct any water deficit, monitor both fluid intake
and output.
Management of Hypernatremia:
21

22. • The goal is to decrease the serum sodium by less than 12 mEq/L
every 24 hours include:
22

23. Food:
• Low potassium intake.
Transcelluler shift:
• Insulin
• β-Adrenergic agonists
Drugs:
• Laxative abuse
• Loop diuretics
• thiazide diuretics
Gastrointestinal tract:
• Emesis/nasogastric suction
• Pyloric stenosis
• Cystic fibrosis
Hypokalemia:
Hypokalemia is defined as a plasma concentration of potassium lower than 3.5
mmol/L (mEq/L).
Etiology:
23

24. Extra renal losses:
• Diarrhea
• Sweating
Renal losses:
• Diabetic ketoacidosis
• Interstitial nephritis
• The diuretic phase of acute tubular
necrosis
• Hypomagnesemia
Others:
• Cushing syndrome
Etiology:
24

25. Musculoskeletal system:
• Muscle weakness and cramps.
• Paralysis usually starts with the legs,
followed by the arms
Respiratory system:
• Respiratory paralysis
Cardiac system:
• Arrhythmias.
GIT system:
• Slows gastrointestinal motility;
GUS System:
• Interstitial nephritis and renal cysts
• Urinary retention
• Impairs bladder function
• Polyuria by producing secondary
nephrogenic diabetes insipidus
Clinical Manifestations
25

26. Investigations:
• Serum potassium level
• Renal function test.
• ECG findings: flattened T wave, depressed ST
segment, presence of Wave, ventricular
fibrillation.
Diagnosis:
• Details History and examination.
26

27. Management of hypokalemia:
• Oral potassium is given in chronic mild cases where
serum K+ is less than 3.5 mEq/L).
• Intravenous (IV) potassium should be used cautiously.
Oral potassium is safer in non-urgent situations. The
dose of IV potassium is 0.5-1 mEq/kg, usually given
over 1 hour. The adult maximum dose is 40 mEq.
• Therapeutic dose of potassium Glauconitic or
potassium chloride ( 2-4mEq /kg /day, divided into 2-4
doses). 27

28. • Frequent monitoring of serum K+ level.
• For patients with excessive urinary losses, potassium-
sparing diuretics are effective.
• Diet (raisin, bananas, tomatoes, fresh oranges and
lemon).
• ECG monitoring. 28

29. Icrease intake:
• Intravenous or oral
• Blood transfusion
Decreased excretion:
• Renal failure
• Primary adrenal disease
• Acquired Addison disease
Hyperkalemia:
Hyperkalemia is defined as a plasma concentration of potassium
more than 5.5 mEq/L (mmol/L).
Etiology:-
29

30. Medications:
• ACE inhibitors
• Angiotensin II blockers
• Potassium-sparing diuretics
• Cyclosporine
• NSAIDs
• Trimethoprim
• β-Adrenergic blockers
Note:-psudohyperkalemia
Spurious Laboratory Value due to
Hemolysis,Tissue ischemia during blood drawing
Thrombocytosis,Leukocytosis .
Etiology:
30
• Transcellular shift
• Acidosis
• Rhabdomyolysis
• Hyperosmolality
• Insulin deficiency
• Malignant
hyperthermia
• Exercisea

31. 31

32. 32

33. • Arrhythmias.
• Palpitation.
• paresthesias, and tingling.
• weakness
• cardiac toxicity usually precedes these
clinical symptoms.
Clinical Manifestations
33

34. Diagnosis:
• Detailed history and examination.
Investigation:
• Serum potassium level.
• RFT.
• ECG changes begin with the peaking of the T waves. As
the potassium level increases, and increased P-R interval,
flattening of the P wave, and widening of the QRS
complex occur; this eventually can progress to ventricular
fibrillation.
34

35. 35

36. Therapy of hyperkalemia has two basic goals:
1-Rapidly decrease the risk of life-threatening arrhythmias:
Shift potassium intracellular:
IV calcium
• Sodium bicarbonate administration (IV)
• Insulin and glucose (IV)
• β-agonist (albuterol via nebulizer)
Management of hyperkalemia:
36

37. 2- Remove potassium from the body :
- loop or thiazide diuretic (IV or PO)
- Sodium polystyrene sulfonate (PO or rectal)
- Dialysis
3- Long-term management of hyperkalemia includes
reducing intake via dietary changes and eliminating
or reducing medications that cause hyperkalemia.
37

39. 39
Thank you